crossing96/oncoscreening huggingface dataset:
Radiotherapy in the management of common genitourinary malignancies.	A continued role for radiation therapy in the multidisciplinary management of genitourinary malignancies seems certain. Treatment outcomes continue to improve, accompanied by diminishing rates of toxicity. With continued technologic advances in the delivery of radiation, including the use of adaptive radiotherapy, the discovery and application of novel treatment agents, and the combined efforts of urologists, medical oncologists, and radiation oncologists, patients who have genitourinary malignancies have an excellent chance of cure.	bladder
Preliminary report on analysis of bladder-wall vasculature using conjunctival microvascular analysis in patients with and without transitional-cell carcinoma.	PURPOSE: To develop a technique to analyze the bladder microvasculature during cystoscopy to assess the conjuctival microvascular morphology at the capillary level. This technique could be an adjunct to visual examination of the bladder during cystoscopy for diseases that are presumed to affect the vasculature. PATIENTS AND METHODS: Subjects with transitional-cell carcinoma (TCC) were chosen because of their frequency of cystoscopy. A total of 12 male patients, ages 45 to 80 years, underwent cystoscopy: four without TCC and eight with TCC by bladder biopsy. The images were digitally recorded and enhanced using a custom image-analysis system. The blood vessel length (VL) and diameter (VD) and blood vessel volume (BVV) were measured. RESULTS: The VD was significantly greater in TCC than in non-TCC patients only in the lower-order vessels. The VL was significantly longer in TCC than in non-TCC, again in the lower-order vessels. In the higherorder vessels, the VL was significantly shorter in TCC than in non-TCC. The BVV in the lower-order vessels was significantly greater in TCC than in non-TCC patients. CONCLUSIONS: Differences exist in the morphology of surface microvessels between TCC and non-TCC bladders. Using the current technique, capillaries (VD < 10 microm) are not visible, so refinement of imaging and recording technologies is required to measure capillaries in order to simulate microvascular morphometry in the conjuctiva.	bladder
Intravesical N-(4-hydroxyphenyl) retinamide and adriamycin induces apoptosis in bladder cancer.	The objective of this study was to evaluate the intravesical application of N-(4-hydroxyphenyl) retinamide (4-HPR) and adriamycin (ADM), as a treatment modality in a an animal model of chemically-induced bladder cancer. Bladder cancer developed in 50.0% of female Wistar rats, 4-6 weeks after intravesical application of the chemical carcinogen, N-methyl-N-nitrosourea (MNU). There was no significant difference in side effects induced by local versus systemic 4-HPR. Although tumor growth was inhibited by 4-HPR and ADM alone, tumor size was lower when both agents were used together. Apoptosis occurred at a higher rate in the combination group than when 4-HPR or ADM was used alone. The results suggest that intravesical use of 4-HPR and ADM may increase their efficacy in treatment of bladder cancer.	bladder
Enhanced urinary bladder and liver carcinogenesis in male CD1 mice exposed to transplacental inorganic arsenic and postnatal diethylstilbestrol or tamoxifen.	Pregnant CD1 mice received 85 ppm arsenite in the drinking water from gestation day 8 to 18, groups (n = 35) of male offspring were subsequently injected on postpartum days 1 through 5 with diethylstilbestrol (DES; 2 microg/pup/day) or tamoxifen (TAM; 10 microg/pup/day), and tumor formation was assessed over 90 weeks. Arsenic alone increased hepatocellular carcinoma (14%), adenoma (23%) and total tumors (31%) compared to control (0, 2 and 2%, respectively). Arsenic alone also increased lung adenocarcinoma, adrenal cortical adenoma and renal cystic tubular hyperplasia compared to control. Compared to arsenic alone, arsenic plus DES increased liver tumor incidence in mice at risk 2.2-fold and increased liver tumor multiplicity (tumors/liver) 1.8-fold. The treatments alone did not impact urinary bladder carcinogenesis, but arsenic plus TAM significantly increased formation of urinary bladder transitional cell tumors (papilloma and carcinoma; 13%) compared to control (0%). Urinary bladder proliferative lesions (combined tumors and hyperplasia) were also increased by arsenic plus TAM (40%) or arsenic plus DES (43%) compared to control (0%) or the treatments alone. Urinary bladder proliferative lesions occurred in the absence of any evidence of uroepithelial cytotoxic lesions. Urinary bladder lesions and hepatocellular carcinoma induced by arsenic plus TAM and/or DES overexpressed estrogen receptor-alpha, indicating that aberrant estrogen signaling may have been a factor in the enhanced carcinogenic response. Thus, in male CD1 mice, gestational arsenic exposure alone induced liver adenoma and carcinoma, lung adenocarcinoma, adrenal adenoma and renal cystic hyperplasia. Furthermore, DES enhanced transplacental arsenic-induced hepatocarcinogenesis. In utero arsenic also initiated urinary bladder tumor formation when followed by postnatal TAM and uroepithelial proliferative lesions when followed by TAM or DES.	bladder
[Changes in the expression of receptors of steroid hormones in the development of partial androgen deficiency of aging men (PADAM)].	This work is devoted to the vital topic of the influence of partial androgen deficiency of aging men (PADAM) on the development of cells with androgen receptors. The results obtained in this study suggest a conclusion that the production of testosterone by some tumors and tissues of the peritumorous zone, which is accompanied by increased proliferative activity and disturbance of the regulation of the cell cycle, is caused by PADAM. The given changes are directed at compensating for testicular deficiency (in particular at overcoming the androgen-dependent stage of development of androgen-sensitive cells). These changes are a partial manifestation of metabolic syndrome (X-syndrome). The atypical cells, which unavoidably develop during metabolic syndrome, are dealt with by means of the immune system, whose capabilities become less and less adequate in the given circumstances.	bladder
LOH at 6p21.3 region and HLA class I altered phenotypes in bladder carcinomas.	Alterations in HLA class I antigen expression have been frequently described in different epithelial tumors and are thought to favor tumor immune escape from T lymphocyte recognition. Multiple molecular mechanisms are responsible for these altered HLA class I tumor phenotypes. Some are structural defects that produce unresponsiveness to treatment with interferons. Others include alterations in regulatory mechanisms that can be switched on by treatment of tumor cells with different cytokines. One important mechanism belonging to the first group is loss of heterozygosity (LOH) at chromosome region 6p21.3, which can lead to HLA haplotype loss. In this investigation, the frequency of LOH at 6p21 chromosome region was studied in 69 bladder carcinomas. Short tandem repeat analysis showed that 35% of cases had LOH in this chromosome region. By considering these results together with immunohistological findings previously published by our group, we identified a distribution pattern of HLA class I altered phenotypes in bladder cancer. The most frequently altered phenotype in bladder carcinomas was total loss of HLA class I expression (17 cases, 25%), followed by phenotype II associated with HLA haplotype loss (12 cases, 17.5%), and HLA allelic loss (ten cases, 14.5%). Nine cases (13%) were classified as having a compound phenotype, five cases (7%) as having HLA locus loss, and in 16 cases (23%) no alteration in HLA expression was detected. An important conclusion of this report is that a combination of different molecular and immunohistological techniques is required to precisely define which HLA alleles are lost during tumor progression and to characterize the underlying mechanisms of these losses. These studies should be performed when a cancer patient is to be included in an immunotherapy protocol that aims to stimulate different immune effector mechanisms.	bladder
[Tumor marker tests in bladder cancer].	The gold standard for detecting bladder cancer is cystoscopy which identifies nearly all papillary and sessile lesions. However, it is an invasive procedure causing some discomfort for patients. Urine cytology is the standard non-invasive marker with very high specificity, but unfavourable poor sensitivity for Ta, G1, and T1 bladder tumors. To improve early detection of bladder cancer as well as to monitor treatment response and tumor recurrence, bladder tumor markers are eligible. An ideal bladder cancer test would have the potential to replace or delay cystoscopy in the follow-up of bladder cancer patients. In recent years, the FDA approved non-invasive tumor marker tests ImmunoCyt / uCyt+, BTA TRAK, BTA stat, NMP22, NMP22 BladderChek, and UroVysion have been investigated. The tests demonstrated higher sensitivity for diagnosis of bladder cancer compared to urine cytology. Overall, the mean sensitivity and mean specificity was 64-80% and 71-95% and the mean positive and negative predictive values to detect malignancy were 49-84% and 79-95%, respectively. BTA TRAK, BTA stat, NMP22, and NMP22 BladderChek assays are limited by false-positive results in patients with benign urological diseases such as hematuria, urocystitis, renal calculi or urinary tract infections. Due to low specificity BTA TRAK, BTA stat, NMP22, and NMP22 BladderChek should not be used without first ruling out benign or malignant genitourinary disease other than bladder cancer. With the exception of UroVysion achieving 80% sensitivity and 94% specificity, none of these non-invasive tests revealed a high sensitivity and specificity at the same time, which is a main demand to be made on an ideal tumor marker. Insufficient sensitivity along with limited specificity does not allow replacing cystoscopy in diagnosis of bladder cancer or treatment decisions based on a positive test result.	bladder
Expression of estrogen receptors-alpha and -beta in bladder cancer cell lines and human bladder tumor tissue.	BACKGROUND: Estrogen receptors (ERs) are known to mediate important physiologic responses as well as the growth of some tumors in response to estradiol stimulation. In a previous study the selective ER modulator raloxifene was shown to induce apoptosis in an ERbeta-positive bladder cancer cell line. However, the expression of ERbeta in human bladder cancer has not been thoroughly investigated. METHODS: ERalpha and ERbeta expression in 224 bladder tumor samples was evaluated using tissue microarray and immunohistochemistry. Levels of ERalpha and ERbeta protein and mRNA expression were determined in several bladder cancer cell lines using quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis. The effect of estradiol and antiestrogen treatments on RT4 bladder cancer cell growth was determined by cell proliferation assays. RESULTS: Analyses revealed that only 2 human bladder cancers weakly expressed ERalpha. In contrast, the expression of ERbeta was detected in 141 tumors (63%). ERbeta was expressed in 58% of WHO Grade 1 and 2 tumors, whereas 70% of Grade 3 tumors demonstrated expression (P = .085). Importantly, although only 53% and 55% of Ta and T1 tumors demonstrated ERbeta expression, 80% of T2, 81% of T3, and 75% of T4 tumors showed ERbeta expression. The differences in ERbeta expression between Ta/T1 and T2/T3/T4 tumors were found to be highly significant (P < .001). Metastatic transitional cell carcinomas had ERbeta expression (80%) comparable to that of muscle invasive bladder cancers. Western blot analysis detected ERbeta protein expression in each of the 5 bladder cancer cell lines tested, whereas no or very low levels of ERalpha were found. Quantitative RT-PCR revealed that higher levels of ERbeta than ERalpha mRNA were present in 5637, T-24, TSU-Pr1, and TCC-Sup bladder cancer cells, whereas ER-alpha mRNA levels were greater than ERbeta in RT4 cells. Treatment with 17beta-estradiol modestly increased RT4 cell growth, whereas the antiestrogens, 4-hydroxtamoxifen, raloxifene, or ICI 182,780 inhibited the growth of RT4 cells. CONCLUSIONS: ERbeta is the dominant receptor expressed in bladder cancer cell lines and in the majority of human bladder tumors. Moreover, the degree of ERbeta expression increases with increasing stage and grade of differentiation. Antiestrogens have an inhibitory effect on the growth of bladder cancer cells in vitro.	bladder
Association of interleukin-1Ra gene polymorphism in patients with bladder cancer: case control study from North India.	OBJECTIVES: To evaluate whether polymorphism of interleukin (IL)-1beta gene (exon 5 and promoter region) and IL-1 receptor antagonist (Ra), 86-bp variable number tandem repeat, are associated with transitional cell carcinoma of the urinary bladder, because cytokines have been hypothesized to be important in cancer development. METHODS: The study included 120 patients with bladder cancer (age range 32 to 69 years) and 150 age-matched controls (age range 25 to 62 years). The polymorphisms were identified by polymerase chain reaction/restriction fragment length polymorphism method and IL-1Ra polymorphism by variable number of identical tandem repeat analysis. Genotype distribution and allelic frequencies between patients and controls were compared. RESULTS: A significant difference was found in the frequency distribution of the IL-1Ra gene polymorphism in patients with bladder cancer compared with the normal control group (P < 0.001), but no difference was found in the frequencies of the IL-1beta promoter region and exon 5 genotypes between patients with bladder cancer and controls (P = 0.112 and P = 0.953, respectively). CONCLUSIONS: This is perhaps the first report on polymorphic changes in gene encoding IL-1Ra in patients with bladder cancer from India. Our data suggest that IL-1Ra intron 2 polymorphism seems to play a prominent role among the IL-1 gene cluster with respect to bladder cancer, and the association studies appear to be plausible in determining the cancer susceptibility and risk.	bladder
Partial cystectomy for muscle invasive urothelial carcinoma of the bladder: a contemporary review of the M. D. Anderson Cancer Center experience.	PURPOSE: Partial cystectomy is a surgical option for select patients diagnosed with urothelial carcinoma. We review our experience with partial cystectomy for muscle invasive urothelial carcinoma to assess local control and survival rates. MATERIAL AND METHODS: From 1982 to 2003 a total of 37 patients with muscle invasive urothelial carcinoma underwent partial cystectomy with curative intent. Reviewed data included history of superficial tumors, presence of variant histology, tumor location, clinical stage, pathological stage, presence of carcinoma in situ, adjuvant therapy and disease status. RESULTS: The 5-year overall, disease specific and recurrence-free survival rates were 67%, 87% and 39%, respectively. Mean followup was 72.6 months (range 6 to 217). Of the 37 patients 19 (51%) did not have tumor recurrence, 9 (24%) had superficial recurrence in the bladder that was treated successfully and 9 (24%) had recurrence with advanced disease. A total of 24 patients (65%) had an intact bladder with no evidence of disease after a median of 53 months. There were 6 patients (16%) who died of bladder cancer, 3 of whom died of late recurrence of muscle invasive cancer (41, 44 and 138 months after partial cystectomy). On multivariate analysis higher pathological stage (HR 3.4, p = 0.04) was associated with shorter recurrence-free survival. A history of superficial tumors (p <0.01) and clinical stage (p = 0.01) was associated with advanced recurrence-free survival. The use of adjuvant chemotherapy (HR 0.18, p = 0.03) was associated with prolonged advanced recurrence-free survival, however adjuvant chemotherapy did not impact overall survival. CONCLUSIONS: Partial cystectomy provides adequate local control of muscle invasive bladder cancer in select patients. Because late recurrence is not uncommon and is potentially life threatening, lifelong followup with cystoscopy is recommended.	bladder
Clinical outcomes following radical cystectomy for primary nontransitional cell carcinoma of the bladder compared to transitional cell carcinoma of the bladder.	PURPOSE: The effect of bladder cancer histological subtypes other than transitional cell carcinoma (nonTCC) on clinical outcomes remains uncertain. We conducted a multi-institutional retrospective study of patients with bladder cancer treated with radical cystectomy to assess the impact of nonTCC histology on bladder cancer specific outcomes. MATERIALS AND METHODS: A total of 955 consecutive patients underwent radical cystectomy with bilateral pelvic lymphadenectomy for bladder cancer at 3 academic institutions. TCC was present in the radical cystectomy specimen in 888 patients (93%). NonTCC histology was present in 67 patients (7%), including squamous cell carcinoma in 26, adenocarcinoma in 13, small cell carcinoma in 10 and other nonTCC subtypes (ie spindle cell carcinoma, carcinosarcoma and undifferentiated carcinoma) in 18. For patients alive at last followup median followup was 39 and 23 months for patients with TCC and nonTCC histologies, respectively. Bladder cancer specific progression and survival were assessed using Kaplan-Meier and multivariate Cox proportional hazards analyses. RESULTS: Bladder cancer specific progression and mortality did not differ significantly between patients with SCC and TCC histologies. Patients with nonTCC and nonSCC bladder cancer were at significantly increased risk for progression and death compared to patients with TCC or SCC (p <0.001). This association remained statistically significant in patients with organ confined disease (stage pT2 or lower) and patients with nonorgan confined disease (stage pT3 or higher) (p <0.001). In a multivariate analysis nonTCC and nonSCC histology was associated with an increased risk of bladder cancer progression and death (OR 2.272 and 2.585, respectively, p <0.001), even after adjusting for final pathological stage, lymph node status, lymphovascular invasion and neoadjuvant or adjuvant treatments. CONCLUSIONS: NonTCC and nonSCC histological subtype is an independent predictor of bladder cancer progression and mortality in patients undergoing radical cystectomy for bladder cancer. Patients with bladder TCC and SCC share similar stage specific clinical outcomes.	bladder
Complications of intravesical therapy for urothelial cancer of the bladder.	PURPOSE: Intravesical therapy is an integral part of treatment in patients with superficial urothelial carcinoma of the bladder. The American Urological Association and European Association of Urology guidelines on bladder cancer incorporate it for the treatment of superficial bladder cancer. Given the extensive use of intravesical immunotherapy and chemotherapy, it is essential for the practicing urologist to be aware of the local and systemic side effects of these therapies. MATERIALS AND METHODS: We reviewed the literature on intravesical immunotherapy and chemotherapy with particular emphasis on side effects, complications and their management. A Medline search of the English language literature for the last 25 years was done on Entrez PubMed and all relevant articles were studied in full. All side effects and complications were studied and their management was reviewed. RESULTS: Intravesical therapy for transitional cell carcinoma of the bladder is generally safe. There is a high incidence of local, usually self-limiting, relatively minor side effects and infrequent, potentially severe local and systemic side effects. Most side effects are avoidable. CONCLUSIONS: Although intravesical therapy is generally safe, local and systemic side effects occur and it is important to be aware of them. Identifying complications early, preventing them when possible and managing them efficiently are critical. Most complications are preventable. Knowing the risks and benefits of chemotherapeutic and immunotherapeutic agents may decrease the short-term and long-term toxicity of these agents. Adherence to guidelines may prevent inappropriate use, which can lead to unnecessary complications, resulting in bladder dysfunction and even cystectomy.	bladder
Kinetics of carboplatin-DNA binding in genomic DNA and bladder cancer cells as determined by accelerator mass spectrometry.	Cisplatin and carboplatin are platinum-based drugs that are widely used in cancer chemotherapy. The cytotoxicity of these drugs is mediated by platinum-DNA monoadducts and intra- and interstrand diadducts, which are formed following uptake of the drug into the nucleus of cells. The pharmacodynamics of carboplatin display fewer side effects than for cisplatin, albeit with less potency, which may be due to differences in rates of DNA adduct formation. We report the use of accelerator mass spectrometry (AMS), a sensitive detection method often used for radiocarbon quantitation, to measure both the kinetics of [14C]carboplatin-DNA adduct formation with genomic DNA and drug uptake and DNA binding in T24 human bladder cancer cells. Only carboplatin-DNA monoadducts contain radiocarbon in the platinated DNA, which allowed for calculation of kinetic rates and concentrations within the system. The percent of radiocarbon bound to salmon sperm DNA in the form of monoadducts was measured by AMS over 24 h. Knowledge of both the starting concentration of the parent carboplatin and the concentration of radiocarbon in the DNA at a variety of time points allowed calculation of the rates of Pt-DNA monoadduct formation and conversion to toxic cross-links. Importantly, the rate of carboplatin-DNA monoadduct formation was approximately 100-fold slower than that reported for the more potent cisplatin analogue, which may explain the lower toxicity of carboplatin. T24 human bladder cancer cells were incubated with a subpharmacological dose of [14C]carboplatin, and the rate of accumulation of radiocarbon in the cells and nuclear DNA was measured by AMS. The lowest concentration of radiocarbon measured was approximately 1 amol/10 microg of DNA. This sensitivity may allow the method to be used for clinical applications.	bladder
Management of panurothelial disease in superficial bladder cancer.	BACKGROUND: A 59-year-old female presented with a history of recurrent superficial bladder cancer. Since the initial diagnosis 12 years earlier, she had had 12 recurrences, all treated with transurethral resection with adjuvant bacillus Calmette-Guérin and mitomycin C. Pathology samples had always shown Ta grade 1 transitional-cell carcinoma. At the last recurrence, she presented with several papillary lesions throughout the bladder, discovered on control cystoscopy. Transurethral resection revealed a papillary grade 3 transitional-cell carcinoma of the bladder. INVESTIGATIONS: Intravenous urography and ureteroscopy. DIAGNOSIS: Panurothelial superficial transitional-cell carcinoma. MANAGEMENT: Radical cystectomy with total right ureterectomy and distal left ureterectomy. Reconstruction of the urinary tract was performed with the distal ileum detubulized and rearranged in a U shape. A pyeloileal anastomosis and a proximal ureteroileal anastomosis were performed at the right and left sides respectively.	bladder